CD5 Specific Neutra™ Antibody Products

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CD5 (also known as LEU1) is a 67-kDa transmembrane glycoprotein, expressed in association with the antigen-specific receptors on the surfaces of a variety of T lymphocytes and B-1a lymphocytes.

In both T-cells and B-cells, CD5 interacts with multiple antigen-specific receptor complexes and regulates their signaling qualitatively or quantitatively. CD5 is initially recognized as a co-stimulatory regulator of T cell activation. In T-cells, the expression of CD5 indicates the strength of antigen receptor signaling, which proportionally modulates the threshold of the subsequent responses. Previous studies have also revealed that CD5 serves as a receptor for pathogen associated molecular patterns and a regulator of cell apoptosis.

Its Gene ID: 921, UniProtKB ID: P06127, and OMIM ID: 153340.

CD5 Functions and Signaling Pathways

CD5 possessed an extracellular region consisting of three SRCR domains. There are some ligands of CD5 have been reported, including CD72, the IgV(H) framework region, as well as polypeptides like gp40-80 and gp150. CD5 is also revealed to exhibit low stoichiometric homophilic properties in cis or trans. Numerous studies have demonstrated that CD5 participates in the activation, differentiation, development, and survival of lymphocytes.

CD5 plays an essential role in the initial signaling in the engagement of the TCR with cognate antigen-MHC complexes in APCs, depending on the functional integrity of the CD5 cytoplasmic domain. When binding of CD5 with its ligands is inhibited, the stimulation of TCR activates CD5 phosphorylation on tyrosine residues and its translocation into the immunological synapse, thus leading to a direct regulation of CD5 by TCR signals.

Fig.1 Signaling pathways of CD5 in DP thymocytes and mature T cells. Fig.1 A model of CD5 signaling in thymocytes and mature T cells.^{1, 3}

There is also a second major signaling domain, the CK2 binding/activation domain, in the cytoplasmic tail of CD5. CD5-CK2 signaling axis is associated with positive selection by triggering the activation of ERK and boosting thymocyte survival independent of proximal TCR signals.

Fig.2 The CD5-CK2 axis involved in thymocyte survival. Fig.2 CD5-CK2 signaling regulates positive selection and maturation of post-selected thymocytes.^{2, 3}

CD5-Targeting Antibodies

CD5 has long been a biomarker of T cell malignancies. CD5 overexpression is observed in about 85% of T cell malignancies, while normal expression of CD5 is restricted to T cells, B1 cells, and thymocytes. In CD5 knockout mice, anti-tumor immunity is reported to be increased, which indicates that inhibiting CD5 on CTLs can be therapeutically effective to enhance the anti-tumor response. Therefore, CD5 has been regarded as a therapeutic targetable tumor antigen, and CD5-targeting therapy has emerged as a promising strategy to treat T cell malignancies. There are multiple CD5-targeting antibodies serving as robust tools in pre-clinical or clinical research projects, or commercially available for cancer treatment.

In recent years, an ex vivo administration in mice of a function-blocking anti-CD5 mAb combined with anti-CD3/anti-CD28 mAbs or 4T1 tumor cell lysates, has been reported to enhance the capacity of primary mouse CTLs to respond to activation. In addition, a bispecific antibody (BsAb) simultaneously targeting CD5 and CD20 has been designed and studied, exhibiting in vivo anti-tumor efficacy by combined activation of redirection of CIK cells to kill the tumor target and innate immunity by Fc.

Creative Biolabs offers different anti-CD5 antibody products. These antibodies are recombinantly expressed and could be used for various purposes. Customization of CD5-based functional antibodies is also available for you here.

REFERENCES

Voisinne, Guillaume, Anne Gonzalez de Peredo, and Romain Roncagalli. "CD5, an undercover regulator of TCR signaling." Frontiers in immunology 9 (2018): 419583.
Mier-Aguilar, Carlos A., et al. "CD5-CK2 signaling modulates Erk activation and thymocyte survival." PLoS One 11.12 (2016): e0168155.
Distributed Under open access license CC BY 4.0, without modification.

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